Leptin receptor gene (LEPR) variants may affect the leptin levels and act as a risk factor for preeclampsia. Two LEPR gene missense variants rs1137101 (c.668A>G) and rs1805094 (c.1968G>C) were investigated in Sudanese women with preeclampsia. A matched case-control study (122 women in each arm) was conducted in Saad Abualila Maternity Hospital in Khartoum, Sudan from May to December 2018. The cases were women with preeclampsia and the controls were healthy pregnant women. Genotyping for LEPR gene variants c.668A>G and c.1968G>C was performed using polymerase chain reaction-restriction fragment length polymorphism. Logistic regression models (adjusted for age, parity, body mass index and hemoglobin level) were conducted. Genotype frequency of LEPR gene variants c.668A>G and c.1968G>C was in accordance with Hardy–Weinberg equilibrium (P > 0.05) in the controls. Allele G in LEPRc.668A>G variant was significantly more frequent in the cases compared with the controls [43.4% vs. 10.2%; OR = 6.44; 95%CI (3.98–10.40); P < 0.001]. In variant LEPRc.668A>G, genotype AG was the prevalent genotype in the cases compared with the controls, and it was significantly associated with preeclampsia risk [37.7% vs. 15.5%; AOR = 3.48; 95%CI (1.15–10.54); P = 0.027]. Likewise, the GG genotype was the second most common genotype in the cases compared with the controls, and was associated with preeclampsia risk [24.6% vs. 2.5%; AOR = 14.19; 95%CI (1.77–113.76); P = 0.012]. None of the LEPRc.1968G>C variant genotypes were associated with preeclampsia. The CC genotype was not detected in neither the cases nor the controls. The haplotype A-G 70.1% was the prevalent haplotype in this population, and it significantly protected against preeclampsia [OR = 0.14; 95%CI (0.09–0.23); P < 0.001]. However, the haplotype G-G 26.8% was significantly associated with preeclampsia risk [OR = 6.70; 95%CI (4.16–11.05); P < 0.001]. Both variants c.668A>G and c.1968G>C were in strong linkage disequilibrium (D′ = 1, r2 = 0.012). Our data indicate that the rs1137101 (c.668A>G) variant and G-G haplotype may independently associate with the development of preeclampsia.

中文翻译：

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苏丹先兆子痫妇女瘦素受体基因多态性c.668A> G和c.1968G> C：病例对照研究。

瘦素受体基因（LEPR）变异可能会影响瘦素水平，并成为先兆子痫的危险因素。在苏丹患有先兆子痫的妇女中研究了两个LEPR基因错义变体rs1137101（c.668A> G）和rs1805094（c.1968G> C）。于2018年5月至2018年12月在苏丹喀土穆的萨阿德阿比维拉产科医院进行了一项匹配的病例对照研究（每组122名妇女）。病例为先兆子痫妇女，对照组为健康孕妇。使用聚合酶链反应-限制性片段长度多态性对LEPR基因变体c.668A> G和c.1968G> C进行基因分型。进行了逻辑回归模型（针对年龄，均等，体重指数和血红蛋白水平进行了调整）。LEPR基因变体c.668A> G和c.1968G>的基因型频率 对照中的C符合Hardy-Weinberg平衡（P> 0.05）。与对照组相比，LEPRc.668A> G变体中的等位基因G的频率明显更高[43.4％比10.2％；或= 6.44; 95％CI（3.98–10.40）；P <0.001]。在变体LEPRc.668A> G中，基因型AG是与对照组相比的常见基因型，并且与先兆子痫风险显着相关[37.7％对15.5％；AOR = 3.48；95％CI（1.15–10.54）；P = 0.027]。同样，GG基因型是该病例中与对照组相比第二常见的基因型，并与先兆子痫风险相关[24.6％vs. 2.5％; AOR = 14.19；95％CI（1.77–113.76）；P = 0.012]。LEPRc.1968G> C变异基因型均与子痫前期无关。在病例和对照中均未检测到CC基因型。AG单体型为70.1％，是该人群中普遍存在的单体型，它能有效预防先兆子痫[OR = 0.14; 95％CI（0.09–0.23）；P <0.001]。然而，单倍型GG 26.8％与先兆子痫风险显着相关[OR = 6.70；95％CI（4.16-11.05）; P <0.001]。变体c.668A> G和c.1968G> C均处于强连锁不平衡状态（D'= 1，r2 = 0.012）。我们的数据表明，rs1137101（c.668A> G）变体和GG单倍型可能与子痫前期的发展独立相关。G和c.1968G> C处于强连锁不平衡状态（D'= 1，r2 = 0.012）。我们的数据表明，rs1137101（c.668A> G）变异和GG单倍型可能与子痫前期的发展独立相关。G和c.1968G> C处于强连锁不平衡状态（D'= 1，r2 = 0.012）。我们的数据表明，rs1137101（c.668A> G）变体和GG单倍型可能与子痫前期的发展独立相关。